Evolution of QRS duration after myocardial infarction: clinical consequences

The natural history of late potentials after acute myocardial infarction (AMI) has been studied in the first 2 years following myocardial infarction (MI). The purpose of the study was to assess the influence of some time delays since MI, including a time delay longer than 2 years on signal-averaged ECG (SAECG). SAECG was recorded at 40-Hz high pass filtering in 40 patients 10 days after acute MI (SAECG 1), then repeated 6-12 months later (mean 9 +/- 3 months) (SAECG 2), and then, 2-4 years later (mean 3 +/- 2 years) (SAECG 3). QRS duration, root mean square voltage of the last 40 ms of QRS (RMS 40), and low amplitude signal duration (LAS) were measured at the first (1), second (2), and third recording (3). Results: (***P < 0.001) [table: see text] The analysis of individual results showed a lengthening QRS duration at the third recording only in patients who had a decreased left ventricular ejection fraction (LVEF) at the third recording. In 12 patients with LVEF > 40%, QRS duration did not change at the first and third recording (104 +/- 15 vs 101 +/- 12 ms). In all 28 patients, but one with LVEF < 40%, QRS duration increased from 107 +/- 12 to 128 +/- 18 ms***. There was no correlation between QRS duration and LVEF at the second recording and no correlation between QRS duration increase at the third recording and the presence or not of late potentials at the first recording. QRS duration lengthening at the third recording was significantly correlated with a left ventricular (LV) dilatation occurrence at the two-dimensional echocardiogram. All arrhythmic events, but two, occurred in patients who developed a QRS duration prolongation and were significantly correlated (P < 0.01) to a mean longer QRS duration (132 +/- 20 ms) than in patients without arrhythmic events (113 +/- 17 ms). In conclusion, the patients with a LV impairment, and who developed a LV dilatation several months after AMI, presented a delayed lengthening of QRS duration noted only at least 2 years after infarction. These patients are at risk of arrhythmic events.     

Prognostic Implications of Loss of Late Potentials Following Acute Myocardial Infarction

The prognosis of patients following myocardial infarction is adversely affected by the finding of late potentials at the time of hospital discharge. Loss of late potentials has been previously reported during seriai testing during the first year after infarction, but it is not known whether such patients remain at risk of arrhythmic events. This study prospectively followed 243 patients after myocardial infarction. Late potentials were observed in 92 patients (group 1) at the time of hospital discharge. Of these patients, 23 no longer had late potentials at G-week follow-up and 8 had had an arrhythmic event (sudden death or ventricular tachycardia). In patients with loss of late potentials, overall QRS duration had decreased from 109 ± 11 msec at discharge to 104 ± 11 msec (P < 0.01), terminal QRS voltage rose from 15 ± 4 μV to 31 ± 9 μV (P = 0.001), and late potential duration fell from 42 ± 6 msec to 28 ± 6 msec (P = 0.001) at the 6-week study. Predictors of loss of late potentials were: initial duration of the QRS duration (P < 0.001) and terminal voltage (P < 0.005); non-Q wave infarction (P < 0.001); and being a male (P < 0.05). After the 6-week assessment, 11 additional arrhythmic events occurred during median follow-up of31 months. The risk of arrhythmic events was similar in patients with loss of late potentials and those who retained late potentials in group I (9% vs 11%, P - NS) but significantly greater than palients with no late potentials at discharge (group II, 2%). Of those patients with events beyond 6 weeks, a normal signal-averaged ECG (either lost late potentials or group II) was observed in 6/11 (55%) patients on at least one occasion prior to the occurrence of the event. Hence, a significant number of arrhythmic events occurring ≥ 6 weeks after myocardial infarction occur in palients with a normal signal-averaged ECG even when late potentials are initially present. “Loss’ of late potentials does not necessarily confer an improved prognosis in terms of risk of arrhythmic events.     

JT Dispersion in Wolff-Parkinson-White Syndrome: Effect of Eccentric Ventricular Depolarization on the Dispersion of Repolarization

There is much interest in QT dispersion for noninvasive risk stratification of patients at risk of arrhythmias. However, little is known about the genesis of abnormal QT dispersion. In particular, whether eccentric ventricular depolarization, as seen in preexcitation, can lead to abnormal dispersion of repolarization is unknown. We studied 24 children aged 1–19 years (mean ± SD, 11 ± 5 years) with manifest preexcitation due to Wolff-Parkinson-White syndrome who had successful catheter ablation. Standard ECGs done preablation, early postablation (< 1 week), mid postablation (> 1 week, < 2 months), and late postablation (> 2 months) were reviewed. The QRS duration prior to ablation ranged from 90–160 ms (mean ± SD, 123 ±21 ms). On the preablation ECG, the JT and JTc dispersions showed no relationship to the QRS duration (r = 0.04 and 0.07, respectively). There was no change in JT dispersion when the preablation (42 ±15 ms) ECG was compared to early (43 ±15 ms), mid (44 ±13 ms), and late postablation (48 ± 19 ms) ECGs. There was no significant change in JTc dispersion as well. Thus, JT dispersion is unrelated to QRS duration and unaffected by catheter ablation in patients with Wolff-Parkinson-White syndrome. Eccentric ventricular depolarization does not lead to abnormal dispersion of repolarization.     

Signal-averaged electrocardiography: a new noninvasive test to identify patients at risk for ventricular arrhythmias

Signal-averaged electrocardiography (ECG) is a new noninvasive test for identifying patients at risk for ventricular arrhythmias. This computerized method of analyzing standard ECGs identifies particular microvolt-level signals called late potentials. Late potentials have been correlated with clinical ventricular tachycardia, are predictive of ventricular tachycardia inducibility at the time of electrophysiologic testing, and are predictive of arrhythmic events after myocardial infarction. In this review, we describe late potentials, the method of obtaining and processing the signal-averaged ECG, and clinical studies in various patient groups that have assessed the predictive value of the signal-averaged ECG for identification of patients at risk for subsequent ventricular arrhythmias.     

Effect of epirubicin-based chemotherapy and dexrazoxane supplementation on QT dispersion in non-Hodgkin lymphoma patients

BACKGROUND AND OBJECTIVE: Aim of the present study was to assess the effect of epirubicin-based chemotherapy on QT interval dispersion in patients with aggressive non-Hodgkin lymphoma (NHL), and the effect of dexrazoxane supplementation. Prolongation of QT dispersion may not only represent a sensitive tool in identifying the first sign of anthracycline-induced cardiotoxicity, but it may serve also in identifying patients who are at risk of arrhythmic events. METHODS: Twenty untreated patients, 相似文献   

A Simple Electrocardiographic Algorithm for Detecting Ventricular Tachycardia

The purpose of this study wus to determine whether a simple ECG algorithm could be developed for predicting susceptibility to ventricular tachyarrhythmias (VT) as defined by sustained spontaneous or inducible VT. Two different QT dispersion algorithms were determined by the difference between the longest and shortest QT interval measured in three orthogonal leads (I, aVF, V1; QTD3), and at least 11 of 12 leads (QTDl2) from the 12-lead ECG. These QT dispersion algorithms were investigated (with and without the QRS duration from the 12-lead EGG) and compared to the signal-averaged ECG (SAEGG) in order to determine their sensitivity and specificity for detecting VT. Only patients who underwent SAECC and were referred for programmed electrical stimulation were included in this study. A positive SAECG was defined by filtered QRS duration > 114 ms, and/or low amplitude signal duration > 38 ms, and/or root mean square voltage in the last 40 ms of < 20 μV. Sixty patients were enrolled in this study with a mean age of 63 ± 2 years. Eifty-five percent of the patients had coronary artery disease. A simple ECG algorithm consisting of the sum of QTD3 plus the QBS duration had a sensitivity and specificity of 90% and 63%. respectively, whereas the SAECG had a sensitivity and specificity of 60% and 63%. respectively (P = 0.022). We conclude that a simple EGG algorithm is more sensitive than the SAEGG for predicting VT. This algorithm combines two easily measured variables obtained from the 12-lead EGG, and can easily be performed without expensive computer equipment.     

QT dispersion in children with ventricular arrhythmia and a structurally normal heart

In adults, increased QT dispersion has been shown to predict arrhythmic risk as well as risk of sudden death in several clinical settings. It is not known whether or not QT dispersion is increased in children with idiopathic ventricular arrhythmia. We studied three groups of children: (1) 20 patients with idiopathic VT (aged 3-18 years; mean 11.2 years); (2) 30 patients with benign PVCs (aged 1-20 years; mean 10.5 years); and (3) 30 control subjects (aged 4-17 years; mean 12 years). Standard ECGs were reviewed and the dispersion of both QT and JT intervals was compared. No patient had structural heart disease or long QT syndrome. The QT and QTc dispersion (QT delta, QTc delta) among the three groups did not differ: QTc delta of the VT group was 70 ms +/- 30 ms, QTc delta of PVC patients was 60 ms +/- 30 ms, and the QTc delta of the control group was 65 ms +/- 30 ms. The JTc delta among the three groups did not differ as well: JTc delta of the VT group was 70 ms +/- 30 ms, the JTc delta of the PVC group was 60 msec +/- 25 msec, and the JTc delta of the control group was 70 ms +/- 30 ms. We conclude that QT and JT dispersion are not significantly altered in children with idiopathic VT or benign PVCs when compared to control subjects. QT dispersion is not a reliable marker for arrhythmic risk in children with idiopathic ventricular arrhythmias and structurally normal hearts.     

QT dispersion and signal-averaged electrocardiogram in hemodialysis and CAPD patients.

OBJECTIVE: The aim of this study was to compare QT dispersion (QTd) and signal-averaged electrocardiogram (SA-ECG) parameters that may predict risk of malignant arrhythmias in patients on hemodialysis (HD), on continuous ambulatory peritoneal dialysis (CAPD), and in controls. SETTING: Controlled cross-sectional study in a tertiary-care setting. PATIENTS: 28 HD (M/F 18/10; mean age 32 +/- 9 years), 29 CAPD (M/F 17/12; mean age 34 +/- 10 years), and 29 healthy controls (M/F 17/12; mean age 32 +/- 8 years) were included. INTERVENTIONS: On ECG, minimum (QTmin) and maximum (QTmax) QT duration and their difference (QTd) were measured. In SA-ECG, duration of filtered QRS, HFLA signals less than 40 microV, and RMS voltage (40 ms) were also measured. RESULTS: Higher serum Ca2+ and lower K+ levels were found in CAPD compared to HD. All QT parameters were increased in HD and CAPD compared to controls. QT dispersion was significantly prolonged in HD compared to CAPD. In HD, QTd was correlated with left ventricular (LV) mass index (r = 0.53, p = 0.004), but not in CAPD (r = -0.09, p = 0.63). QT dispersion was significantly prolonged in patients with LV hypertrophy compared to patients without hypertrophy on HD (68 +/- 18 ms vs 49 +/- 18 ms, p = 0.008). In the analysis of SA-ECG, 3 of the 28 (11%) HD and 2 of the 29 (7%) CAPD patients had abnormal late potentials. Patients on HD and CAPD had significantly higher filtered-QRS duration compared to controls (105 +/- 15 ms and 104 +/- 12 ms vs 95 +/- 5 ms, respectively, p = 0.04). Patients with LV hypertrophy had higher filtered-QRS duration compared to patients without hypertrophy (109 +/- 12 ms vs 95 +/- 8 ms, p < 0.001). CONCLUSION: Dialysis patients had prolonged QTd and increased filtered-QRS duration in SA-ECG compared to controls. Patients on HD had longer QTd than patients on CAPD. QTd has been correlated to LV mass index in HD, but not in CAPD. This difference might be due to the effect of different dialysis modalities on electrolytes, especially the higher serum Ca2+ levels.     

QRS duration in high-resolution methods and standard ECG in risk assessment after first and recurrent myocardial infarctions

Background: Prolonged QRS duration (QRSd) is associated with increased mortality after myocardial infarction (MI). Only little data exist about its predictive ability and relationships to clinical variables in the present era of active treatment of myocardial ischemia and cardiac dysfunction. We investigated whether QRSd in high-resolution methods and standard ECG predict arrhythmic events and cardiac death in post-infarction patients with cardiac dysfunction and how it relates to clinical variables, with a special emphasis on history of previous MI.
Methods and Results: Patients (n = 158) with acute MI and cardiac dysfunction had magnetocardiography (MCG), signal-averaged ECG (SAECG), and ECG registered at discharge. Patients with a previous MI had significantly longer QRSd although their left ventricular function was almost similarly impaired. During the mean follow-up of 50 ± 15 (range 1–72) months, 32 patients died and 17 (53%) of the deaths were classified as cardiac. Eighteen patients had an arrhythmic event. QRSd >121 ms in MCG and >114 ms in SAECG were significant predictors of arrhythmic events and cardiac death, whereas QRSd in ECG predicted only cardiac death. In multivariate analysis, QRSd in MCG (hazard ratio (HR) = 3.6, P = 0.007) and SAECG (HR = 4.6, P = 0.016) predicted only arrhythmic events, whereas QRSd in ECG was an independent predictor of cardiac death.
Conclusions: Prolonged QRSd in MCG and SAECG are powerful indicators of the arrhythmia substrate in post-infarction patients with cardiac dysfunction, whereas prolonged QRSd in standard ECG associates with increased risk of cardiac death.     

Different Effects of Amiodarone and Quinidine on the Homogeneity of Myocardial Refractoriness in Patients With Intraventricular Conduction Delay

BACKGROUND: Increases in QT and JT dispersion have been suggested as indicative of a proarrhythmic potential as a result of heterogeneity in myocardial refractoriness, the reduction of which by antiarrhythmic agents might be associated with a beneficial effect on the development of serious ventricular arrhythmias. METHODS: To test the hypothesis that amiodarone reduces the heter-ogeneity of ventricular refractoriness to a significantly greater extent than quinidine in patients with intraventricular conduction defects under treatment for ventricular arrhythmias, the corrected and uncorrected QT and JT intervals and dispersions from 12-lead surface electrocardiograms were determined in 120 patients with intraventricular conduction defects with cardiac arrhythmias before and during treatment with amiodarone (n = 60) and quinidine (n = 60). RESULTS: Amiodarone increased QT from 403 +/- 50 ms to 459 +/- 47 ms (P <.001), with a similar increase in the corrected QT interval (QTc) (P <.001). Amiodarone reduced QT dispersion by 40% (P <.001), whereas quinidine increased by 18% (P <.001). The net effects of both drugs were similar for OTc. Amiodarone, but not quinidine, reduced heart rate significantly; amiodarone had no effect on the QRS; but quinidine increased if (P <.001). Quinidine as well as amiodarone increased the JT and JTc intervals significantly, but the effect of quinidine was qualitatively less striking. Amiodarone decreased the JT dispersion by 33% (P <.001) and JTc dispersion by 37% (P <.001). On the other hand, quinidine increased the corresponding values for JT and JTc by 18% (P <.001) and 21% (P <.001), respectively. The overall data on QT and JT dispersion indicate an improvement in the homogeneity of myocardial refractoriness with amiodarone treatment and the converse with quinidine treatment; this observation is consistent with a lower proarrhythmic propensity and mortality with amiodarone than with quinidine. Quinidine increased the QRS interval more than amiodarone, and the data indicate that in patients with intraventricular conduction defects, the monitoring of the JT interval might more accurately reflect changes in myocardial repolarization. CONCLUSIONS: Amiodarone and quinidine both increased the corrected and uncorrected QT and JT intervals; amiodarone decreased and quinidine increased the dispersion of these intervals, and these results suggested an improvement in the homogeneity of myocardial refractoriness as a result of amiodarone treatment and the converse as a result of quinidine treatment. Quinidine increased the QTS interval more than amiodarone, and the data indicate that in patients with intraventricular conduction defects, the monitoring of the JT interval might more accurately reflect changes in myocardial repolarization.     

Influence of electrolyte abnormalities on interlead variability of ventricular repolarization times in 12-lead electrocardiography

Increased QT dispersion (QT(d)) has been associated with increased risk for ventricular arrhythmias. Pathologic extracellular electrolyte concentrations may result in ventricular arrhythmias. The aim of this study was to evaluate the effect of electrolyte abnormalities on QT(d). Ten consecutive patients with isolated electrolyte abnormalities were selected for each of the following groups: hypokalemia, hyperkalemia, hypercalcemia, hypocalcemia, hypomagnesemia, and normal controls. Standard 12-lead electrocardiography was performed for each patient and average QT, JT, and RR intervals were calculated for each lead. Dispersion of QT, JT (JT(d)), and QTc (QTc(d)) intervals were calculated as the range between the longest and shortest measurements. Compared with controls, only patients with hypokalemia had a greater QT(d) (115 +/- 31 vs. 49 +/- 15 ms), JT(d) (116 +/- 34 vs. 52 +/- 12 ms), and QTc(d) (141 +/- 40 vs. 58 +/- 1 ms), (P < 0.05). In an experimental substudy, seven rats were maintained on K(+) and seven on Mg(2+)-free diet followed by normal diet. Experimental hypokalemia significantly increased QT(d) (10 +/- 4 to 37 +/- 7 ms), and QTc(d) (32 +/- 6 to 79 +/- 27 ms) (P < 0.05), whereas hypomagnesemia did not. Restoration of serum potassium resulted in normalization of dispersion (QT(d), 14 +/- 2; QTc(d), 34 +/- 6 ms). Hypokalemia increases the dispersion of ventricular repolarization that may be responsible for arrhythmias. Even though hyperkalemia, hypocalcemia, and hypercalcemia are known to affect ventricular repolarization, our study shows that they are not associated with increased dispersion.     

Clinical Significance of Increased QT Dispersion in the 12-Lead Standard ECG for Arrhythmia Risk Prediction in Dilated Cardiomyopathy

QT dispersion was determined from the 12-lead standard ECGs from 107 patients with idiopathic dilated Cardiomyopathy (IDC) and compared to QT dispersion measurements in 100 healthy age and sex matched controls. QT dispersion, rate corrected QT dispersion and adjusted QT_C dispersion were significantly greater in patients with IDC compared to controls. During a prospective follow-up of 13 ± 7 months, arrhythmic events, defined as sustained VT, VF, or sudden death, occurred in 12 (11%) of 107 study patients with IDC. QT dispersion was increased in patients with arrhythmic events compared to patients without arrhythmic events during follow-up (76 ± 17 vs 60 ± 26 ms; P = 0.03). Differences in QT_C dispersion and adjusted QT_C dispersion between patients with and without arrhythmic events, however, failed to reach statistical significance. Thus, although QT dispersion was increased in patients with IDC and arrhythmic events during follow-up, its clinical usefulness for risk stratification appears to be very limited due to the large overlap of QT dispersion among patients with and without arrhythmic events.     

QT dispersion from body surface ECG does not reflect the spatial dispersion of ventricular repolarization in sheep

The correlation between the QT dispersion on body surface ECG and the dispersion in ventricular repolarization from the cardiac surface was studied in six sheep anesthetized with pentobarbital. The standard 12-lead body surface ECG and multiple ventricular epicardial ECGs were simultaneously recorded. The activation-recovery interval (ARI) was measured from the unipolar epicardial ECGs. The pooled QT dispersion from the six animals was significantly smaller than the pooled ARI dispersion (22.7 +/- 2.6 vs 33.0 +/- 6.9 ms, P < 0.01). There was no correlation between the QT and ARI dispersion. The unipolar epicardial ECGs were then converted into bipolar ECGs and epicardial QT intervals were subsequently acquired from these ECGs. The average value of epicardial QT dispersion from the six animals was similar to that of body surface ECG, but was less than the ARI dispersion (27.5 +/- 6.8 vs 33.0 +/- 6.9, P < 0.01). A good correlation between the epicardial QT dispersion and ARI dispersion was identified (r = 0.84, P < 0.05). In addition, a prolongation in ventricular repolarization, induced by an increase in coronary flow, elicited a pooled ARI dispersion of 62.3 +/- 6.2 ms (n = 6), which was larger than the simultaneously recorded body surface QT dispersion (28.3 +/- 9.8 ms, n = 6, P < 0.01). No correlation between the ARI and QT dispersion was found in the presence of the prolonged ventricular repolarization. In conclusion, QT dispersion from a 12-lead body surface ECG seems to underestimate the spatial dispersion of ventricular repolarization acquired from sheep epicardium.     

Spatial distribution of repolarization times in patients with coronary artery disease

The potential clinical value of QT dispersion (QTd), a measure of the interlead range of QT interval duration in the surface 12-lead ECG, remains ambiguous. The aim of the study was the temporal and spatial analysis of the QT interval in healthy subjects and in patients with coronary artery disease (CAD) using magnetocardiography (MCG) and surface ECG. Standard 12-lead ECG and 37-channel MCG were performed in 20 healthy subjects, 23 patients with CAD without prior myocardial infarction (MI), 31 MI patients and 11 MI patients with ventricular tachycardia (VT). QTd was increased in CAD without MI compared to normals (ECG 46.1 +/- 6.0 vs 42.8 +/- 5.0, P < 0.05; MCG 66.8 +/- 20.3 vs 49.7 +/- 10.8, P < 0.01) and in VT compared to MI (ECG 66.8 +/- 16.5 vs 51.9 +/- 16.6, P < 0.05; MCG 93.6 +/- 29.6 vs 66.8 +/- 20.8, P < 0.005). In MCG, spatial distribution of QT intervals in patient groups differed from those in healthy subjects in three ways: (1) greater dispersion, (2) greater local variability, and (3) a change in overall pattern. This was quantified on the basis of smoothness indexes (SI). Normalized SI was higher in CAD without MI compared to normals (3.8 +/- 1.1 vs 2.7 +/- 0.6, P < 0.001) and in VT compared to MI (6.4 +/- 1.6 vs 4.2 +/- 1.4, P < 0.0005). For the normal-CAD comparison a sensitivity of 74% and a specificity of 80% was obtained, for MI-VT, 100% and 77%, respectively. The results suggest that examining the spatial interlead variability in multichannel MCG may aid in the initial identification of CAD patients with unimpaired left ventricular function and the identification of post-MI patients with augmented risk for VT.     

Impact of electrocardiogram recording format on QT interval measurement and QT dispersion assessment

The aim of this study was to determine the effect of recording conditions on the operator dependent measures of QT dispersion in patients with known and/or suspected repolarization abnormalities. Among several methods for risk stratification, QT dispersion has been suggested as a simple estimate of repolarization abnormalities. In a cohort of high and low risk patients, different components of the repolarization process were assessed in the 12-lead ECG using three different paper speeds and amplifier gains. To assess measurement error and reproducibility, a straight line was repeatedly measured. The operator error was 0.675 +/- 0.02 mm and the repeatability of the measurement error was 31 +/- 6%. The QT interval was most frequently measurable in V2-V5. Depending on the lead selected for analysis, the incidence of visible U waves was greatest in the precordial leads with high amplifier gain and low paper speed, strongly affecting QT interval measurement. The timing of the onset of the QRS complex (QRS onset dispersion) or offset of the T wave was strongly dependent on the paper speed. Paper speed, but not amplifier gain, had a significant shortening effect on the measurement of the maximum QT interval. As QT interval measurement in each ECG lead incorporates QRS onset and T wave offset (depending on the number of visible U waves), the dispersion of each of these parameters significantly affected QT dispersion. Thus, QT dispersion appears to reflect merely the presence of more complex repolarization patterns in patients at risk of arrhythmias.     

Noninvasive Arrhythmia Risk Stratification in Idiopathic Dilated Cardiomyopathy: Design and First Results of the Marburg Cardiomyopathy Study

The Marburg Cardiomyopathy Study (MACAS) is a prospective, observational study designed to determine the value of the following potential noninvasive arrhythmia risk predictors in at least 200 patients with idiopathic dilated Cardiomyopathy (IDC) over a 5-year follow-up period: NYHA-class, left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter, left bundle branch block and atrial fibrillation on ECG, QT/JT dispersion on 12-lead ECG, signal-averaged ECG, ventricular arrhythmias and heart rate variability (HRV) on 24-hour Hotter ECG, baroreflex sensitivity, and microvolt T wave alternans during exercise. This article describes the findings among the first 159 patients with IDCs enrolled in MACAS until May 1998 (40 women, 119 men;age:49 ± 12 years; LVEF: 32 ± 10%). Twenty-nine patients (18%) had atrial fibrillation and 130 patients (82%) were in sinus rhythm. Patients with sinus rhythm were further stratified according to LVEF < 30% (n = 54) versus LVEF ≥ 50% (n = 76). Compared to patients with LVEF ≥ 30%, patients with LVEF < 30% more often had left bundle branch block (43% vs 25%, P < 0.05), nonsustained VT (44% vs 22%, P < 0.05), decreased HRV (SDNN: 95 ± 39 vs 128 ± 42 ms, P < 0.01), decreased baroreflex sensitivity (5.6 ± 4 vs 8.3 ± 6 ms/mmHg, P < 0.01), and T wave alternans (59% vs 37%, P < 0.05). The prognostic significance of these findings will be determined by multivariate Cox analysis at the end of a 5-year follow-up. Primary endpoints in MACAS are overall mortality and arrhythmic events (i.e., sustained VT or VF, or sudden cardiac death).     

Transient proarrhythmic state following atrioventricular junctional radiofrequency ablation

This study was designed to prospectively assess ventricular de- and repolarization by the QRS, QT, and JT intervals, and their dispersion in the 12-lead ECG during right ventricular pacing at 60, 70, and 80 beats/min during the first month after AV junctional RF ablation. Previous reports have found early polymorphic ventricular arrhythmia after RF AV junctional ablation. Our hypothesis was that there is a proarrhythmic state following this procedure, which depends on the paced rate and time after ablation. The analysis of the immediate changes was based on 17 patients (10 men) with a mean age of 64 years (SD 14) (range 38-82 years). A 12-lead ECG was recorded during right ventricular pacing at 60, 70, and 80 beats/min within 24 hours (day 1), between 24 and 48 hours (day 2), and 1 week after ablation (day 7). For analysis of changes beyond 1 week, 13 additional patients with a mean age of 73 years (SD 8) (range 62-90 years) were analyzed on days 1, 7, and 30. All intervals were measured with a digitizing table. The mean QRS duration shortened by 2.4% at 60 beats/min (P <0.01), and the mean QT and JT intervals shortened by 5-7% between days 1 and 7 (P < 0.001). The mean QT was 9% shorter and the mean JT interval was 13% shorter at 80 compared to 60 beats/min on day 1 (P < 0.001). QT dispersion was reduced by 13% when the stimulation rate was increasedfrom 60 to 80 beats/min on day 1 (P < 0.05). There were no significant changes beyond the first week. The study results point to the induction of a proarrhythmic state immediately after AV junctional RF ablation resolving during the first week. Repolarization shortened gradually between 80 and 60 beats/min to an extent that is suggestive of a clinically important antiarrhythmic effect at the higher rate, which was supported also by clinical experience.     

Spectrotemporal Mapping of High-Resolution ECGs in Experimental Myocardial Infarction: Comparison with Time-Domain Analysis and Epicardial Electrograms

The study was undertaken to evaluate the relationship of signal-averaged ECG (SA-ECG) readings in the frequency domain (STM) and epicardial electrograms (EE) recorded before and after acute myocardial infarction (AMI) in pigs and to compare the changes with findings in time-domain analysis (TDA). In 20 pigs the left anterior descending artery (LAD) was ligated. Prior to ligation, a SA-ECG was recorded (method of Simson) and bipolar electrodes were used to register EE in the areas supplied by the LAD and the circumflex artery (CIRC). Five minutes after LAD ligation, all measurements were repeated. Time-domain parameters were QRS duration (QRS D) and the duration of the signal below 30 microV (LAS 30). Beginning at a point of 20 ms before the QRS end, the frequency spectra (0-200 Hz) of 25 segments of 80-ms duration at the QRS end were analyzed. The volumes below the 25 curves were analyzed separately for 0-50 Hz, 51-100 Hz, 101-150 Hz, and 151-200 Hz. After AMI, five pigs died within 7 minutes. In 15 pigs, QRS D as well as LAS 30 lengthened significantly (P<0.05; P<0.001). Spectrotemporal mapping (STM) showed a significant decrease of the frequencies above 50 Hz (51-200 Hz) in the entire group and in the animals with late potentials (P<0.05). EE of the LAD area were significantly prolonged (P<0.01); this did not correlate with the changes in STM parameters. In pigs acute myocardial infarction causes a shift towards lower frequencies in the STM which most likely reflects the slowed depolarisation in the ischemic area.     

Incidence of T Wave Alternation After Acute Myocardial Infarction and Correlation with Other Prognostic Parameters: Results of a Prospective Study

Tachycardia induced alternation of the T wave (TWA) has been associated with arrhythmia morbidity in mixed patient populations. However, less is known concerning the general incidence of TWA and its usefulness in risk stratification early after acute myocardial infarction (MI). TWA was prospectively and systematically assessed in 140 consecutive patients 15 +/- 6 days after acute MI and prior to discharge. Results of TWA measurements were compared to other noninvasive risk markers, LV function, and coronary angiography. Sustained TWA was present at rest or inducible during exercise in 27% of patients. The patient-specific heart rate for the onset of TWA was 98 +/- 9 beats/min. After multivariate analysis, TWA correlated with age (P = 0.02) and LV function (P = 0.002) and occurred more often in patients after nonanterior MI (P = 0.03). Acute results of Holter monitoring, late potentials by signal-averaged ECG, and heart rate variability were unrelated to the TWA status. During follow-up (451 +/- 210 days) two major arrhythmic events occurred. The incidence of TWA early after MI is about 25%. TWA is related to age and LV function but not to other common arrhythmia markers. Although TWA does not appear to be related to excessive cardiac morbidity, evaluation of the prognostic significance of TWA requires further study.     

Effect of thrombolytic therapy on QT dispersion in elderly versus younger patients with acute myocardial infarction

The objective of this study was to assess the degree of QT dispersion and effect of thrombolytic therapy on QT dispersion in elderly (age > or =65 years) versus younger (age <65 years) patients with acute myocardial infarction. The QT dispersion was measured manually in 10 +/- 2 leads of 12-lead electrocardiograms on admission, at completion of thrombolytic therapy, and at day 2 after thrombolytic therapy in 36 elderly (73 +/- 5.7 years) and 36 younger (59.9 +/- 7.7 years) patients with acute myocardial infarction. Before initiation of thrombolytic therapy, elderly patients had higher absolute and corrected QT dispersion than younger patients (absolute QT dispersion: 76.3 +/- 7.3 versus 69.6 +/- 7.5 milliseconds, respectively, P < 0.0001; corrected QT dispersion: 77.9 +/- 7.6 versus 70.8 +/- 7.4 milliseconds, respectively, P < 0.001). The difference in QT dispersion between elderly and younger patients persisted at the completion of thrombolytic therapy (absolute QT dispersion: 75.1 +/- 7.2 versus 69.1 +/- 8.4 milliseconds, respectively, P = 0.001; corrected QT dispersion: 77.2 +/- 7.2 versus 70.7 +/- 8.0 milliseconds, respectively, P = 0.001) and at day 2 after thrombolytic therapy (absolute QT dispersion: 74.1 +/- 8.2 versus 69 +/- 9.1 milliseconds, respectively, P = 0.01; corrected QT dispersion: 76.0 +/- 7.9 versus 70.5 +/- 8.8 milliseconds, respectively, P = 0.006). Compared with the prethrombolytic values, there was no significant change in absolute and corrected QT dispersion at the completion of thrombolytic therapy or at day 2 after thrombolytic therapy in elderly or younger patients. Elderly patients with acute myocardial infarction have higher QT dispersion than younger patients with acute myocardial infarction, and QT dispersion does not change early after thrombolytic therapy in elderly or younger patients.